Evidence map›Paper›PMID 26108570›Full record

ArticleThorax2015

Toll-like receptor 7 governs interferon and inflammatory responses to rhinovirus and is suppressed by IL-5-induced lung eosinophilia.

Luke Hatchwell, Adam Collison, Jason Girkin, Kristy Parsons, Junyao Li, Jie Zhang, Simon Phipps, Darryl Knight, Nathan W Bartlett, Sebastian L Johnston and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thorax, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
7.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 107 citations in OpenAlex.

  1. Lower viral loads in subjects with rhinovirus-challenged allergy despite reduced innate immunity.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022
    Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025
    Review
  7. Article
  8. The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Living without eosinophils: evidence from mouse and man.The European respiratory journal · 2023
    Review
  16. Review
  17. Review
  18. T-helper 2 mechanisms involved in human rhinovirus infections and asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022
    Review
  19. Toll-like receptor-agonist-based therapies for respiratory viral diseases: thinking outside the cell.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Luke HatchwellDepartment of Experimental & Translational Respiratory Medicine, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Adam CollisonDepartment of Experimental & Translational Respiratory Medicine, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Jason GirkinDepartment of Experimental & Translational Respiratory Medicine, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.ORCID http://orcid.org/0000-0002-0739-1070
Kristy ParsonsPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, New South Wales, Australia.
Junyao LiDepartment of Experimental & Translational Respiratory Medicine, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Norman Bethune Medical Science Centre, Jilin University, Jilin, Changchun, China.
Jie ZhangNorman Bethune Medical Science Centre, Jilin University, Jilin, Changchun, China.
Simon PhippsThe School of Biomedical Sciences, University of Queensland, Queensland, Queensland, Australia.
Darryl KnightPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Nathan W BartlettAirway Disease Infection Section, National Heart and Lung Institute, Medical Research Council & Asthma UK Centre in Allergic Mechanisms of Asthma, Imperial College London, Norfolk Place, London, UK.
Sebastian L JohnstonAirway Disease Infection Section, National Heart and Lung Institute, Medical Research Council & Asthma UK Centre in Allergic Mechanisms of Asthma, Imperial College London, Norfolk Place, London, UK.
Paul S FosterPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Peter A B WarkPriority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, New South Wales, Australia.
Joerg MattesDepartment of Experimental & Translational Respiratory Medicine, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia Department of Paediatric Respiratory and Sleep Medicine, Newcastle Children's Hospital, Newcastle, New South Wales, Australia.
Hunter Medical Research Institute · AUAsthma UK · GBJohn Hunter Hospital · AUFirst Bethune Hospital of Jilin University · CNThe University of Queensland · AU

Funding

Medical Research Council 1011153Medical Research Council G1000758
6 · The paper itself

Abstract

backgroundAsthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), which is sensed by Toll-like receptors (TLR) such as TLR7. Some asthmatics have impaired interferon (IFN) responses to RV, but the underlying mechanisms of this clinically relevant observation are poorly understood.

objectivesTo investigate the importance of intact TLR7 signalling in vivo during RV exacerbation using mouse models of house dust mite (HDM)-induced allergic airways disease exacerbated by a superimposed RV infection.

methodsWild-type and TLR7-deficient (Tlr7(-/-)) BALB/c mice were intranasally sensitised and challenged with HDM prior to infection with RV1B. In some experiments, mice were administered recombinant IFN or adoptively transferred with plasmacytoid dendritic cells (pDC).

resultsAllergic Tlr7(-/-) mice displayed impaired IFN release upon RV1B infection, increased virus replication and exaggerated eosinophilic inflammation and airways hyper reactivity. Treatment with exogenous IFN or adoptive transfer of TLR7-competent pDCs blocked these exaggerated inflammatory responses and boosted IFNγ release in the absence of host TLR7 signalling. TLR7 expression in the lungs was suppressed by allergic inflammation and by interleukin (IL)-5-induced eosinophilia in the absence of allergy. Subjects with moderate-to-severe asthma and eosinophilic but not neutrophilic airways inflammation, despite inhaled steroids, showed reduced TLR7 and IFNλ2/3 expression in endobronchial biopsies. Furthermore, TLR7 expression inversely correlated with percentage of sputum eosinophils.

conclusionsThis implicates IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression and antiviral responses, which provides a molecular mechanism underpinning the effect of eosinophil-targeting treatments for the prevention of asthma exacerbations.

Indexed as

AnimalsEosinophilsFlow CytometryHumansInflammationInterferonsInterleukin-5LungMaleMembrane GlycoproteinsMiceMice, Inbred BALB CPicornaviridae InfectionsPulmonary EosinophiliaPyroglyphidaeReal-Time Polymerase Chain ReactionInterferonsInterleukin-5Membrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7AsthmaInnate ImmunityPulmonary eosinophiliaRespiratory Infection

Identifiers

PMID26108570
PMCPMC4552894
OpenAlexW2163635921

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.